P53 is a tumour suppressor gene, located in the short arm of chromosom
e 17, which encodes for a nuclear protein involved in the control of c
ellular growth, regulating the entry of the cell into the S-phase. P53
mutations have been identified in a progressively increasing number o
f human malignancies. Nuclear p53 protein is usually present in non-tu
mour cells in minute concentrations, due to its short half-life. In co
ntrast, tumours with p53 mRNA mutations show a higher nuclear protein
concentration, detectable by immunohistological techniques, due to sta
bilization by complexing with other proteins such as heat-shock protei
n or wild-type p53 protein. Levels of nuclear p53 protein detected by
immunohistochemistry with the monoclonal antibody PAb 1801 were measur
ed with the aid of an image analysis system in 83 non-Hodgkin's lympho
mas (NHLs) and 13 cases of Hodgkin's disease, as well as in 14 cases o
f normal thymus, reactive tonsils, and lymphadenitis. High levels of p
53 protein (> 5 per cent of the cells) were present only in high-grade
lymphomas (in the proportion 13/55), with a peak incidence in Burkitt
's lymphoma (5/8 cases). Lower levels (< 5 per cent) of p53 protein we
re detected in low-grade B- and T-cell lymphomas, as well as in most o
f the cases of Hodgkin's disease, where p53 protein was selectively pr
esent in Hodgkin and Reed-Sternberg cells. In 5/14 reactive tonsils or
lymph nodes, occasional p53-positive cells were identified. These res
ults suggest a relationship between levels of p53 protein and the aggr
essiveness of NHL. The sporadic presence of p53-positive cells in huma
n reactive tissues suggests that its expression could depend not only
on mutation, but also on stabilization of the protein through complexi
ng with other nuclear proteins. It is not known if this mechanism is a
lso responsible for the p53 nuclear accumulation in high-grade lymphom
as.